半胱氨酸蛋白酶atg4b执行两个lc3/gabarap处理事件：启动新合成的pro-lc3/gabarap以实现脂化(新翻译的lc3b，称为pro-lc3，在c-末端被半胱氨酸蛋白酶atg4b切割，得到lc3-i)和在自溶酶体中货物降解后脂化lc3/gabarap的去调节（fig.4）。

Furthermore, to increase selective targeting of RavZ-based sensors into LC3- or GABARAP-positive autophagic membranes, we replaced the LIR motifs of RavZ with selective LC3- or GABARAP subfamily-binding LIR motifs and developed additional RavZ-based probes that were selectively detecting for LC3- or GABARAP-positive autophagic membranes in cells.

通过Western印迹定量LC3蛋白的表达和直接mTORC1靶标p70S6K1-T389的磷酸化。 使用共聚焦荧光成像，lysotracker，和活细胞成像。 RAP减少了PA诱导的细胞凋亡。

2025年3月20日 · A3Bp shows a much more attenuated increase in GFP-LC3 puncta formation in the presence of Rap (Figure 4 D), which highlights the importance of building block 220 (Figure 2 D) and is consistent with the screening results.

Download scientific diagram | Effects of 3-MA Rap on LC3 and active caspase 3 in H9c2 cells. H9c2 cells were treated with 3-MA for 24 h or Rap for 12 h under normal conditions and for 150 min...

RAP can effectively inhibit the mTOR/P70S6K/4EBP1 signaling pathway, and activate podocyte autophagy, consequently reducing podocyte apoptosis. Therefore, RAP could be used for the treatment of idiopathic membranous nephropathy.

To better characterize this assay in mammalian cells, HeLa cells stably expressing GFP-LC3 were treated with rapamycin (Rap), a well-known autophagy inducer by suppressing mTOR, 26 for different concentrations and time points. Rap increased the number of GFP-LC3 puncta in a concentration-dependent manner (Fig. 1A and B).

因此,本研究建立脂多糖(LPS)所 致脓毒症急性肺损伤模型,分别用自噬促进剂雷帕霉素(rapamycin,RAP)和自噬抑制剂3 甲 基腺嘌呤(3 methyladenine,3 MA)干预,观 察自噬的改变和脓毒症肺损伤的关系。 1 1 试剂雷帕霉素(rapamycin,RAP,纯 度大于98%)、3 甲 基腺嘌呤(3 methyladenine,3 MA,纯 度>98%)、脂...

2016年1月12日 · ATGL exhibits LC3-interacting region (LIR) motifs, and mutating a single LIR motif on ATGL displaces ATGL from LD and disrupts lipolysis. Thus, cold-induced activation of central autophagy activates lipophagy and cytosolic lipases in a complementary manner to mediate lipolysis in peripheral tissues.

2023年11月23日 · WB结果证实，在海马和/或 皮 层 组 织中，GP17、RAP 和/或 3-MA 增 加 了Beclin1 和 LC3-B 的表达，抑制了 P62 的表达(图 2E-I)。 透射电镜（TEM）结果显示 MCAO/R 诱导了自噬小体的积累，而 GP-17、RAP 和 3-MA 处理促进了多个自噬空泡的形成(图2J)。